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富氢盐水可减少实验性一氧化碳中毒的迟发性神经后遗症。

Hydrogen-rich saline reduces delayed neurologic sequelae in experimental carbon monoxide toxicity.

机构信息

Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.

出版信息

Crit Care Med. 2011 Apr;39(4):765-9. doi: 10.1097/CCM.0b013e318206bf44.

Abstract

OBJECTIVE

We investigated the feasibility and efficacy of hydrogen-rich saline therapy on delayed neurologic sequelae in a rat model of severe acute carbon monoxide (CO) poisoning.

DESIGN

Controlled animal study.

SETTING

University research laboratory for Diving Medicine.

SUBJECTS

Sprague-Dawley rats weighing 250 ± 20 g.

INTERVENTIONS

The rats were exposed to 1000 ppm CO in air for 40 min and then to 3000 ppm for another 20 min until they lost consciousness. Rats were intraperitoneal injected with hydrogen-rich saline or normal saline (10 mL/kg) for six times after resuscitation at 0, 12, 24, 36, 48, and 60 hrs, respectively. The rats without CO poisoning were used as normal controls.

MEASUREMENTS AND MAIN RESULTS

Brain tissue inflammation, cell death, and cognitive dysfunction were observed at one week after CO poisoning. Hydrogen-rich saline treatment significantly reduced the level of degraded myelin basic protein, decreased the expression of ionized calcium-binding adapter molecule 1, Iba1, a microglial marker, reduced DNA oxidation, and suppressed proinflammatory cytokine interleukin-1β, interleukin-6, and tumor necrosis factor-α in the cortex and hippocampal tissues when compared with those in normal saline-treated rats. These histologic and biological improvements were accompanied with an improvement in the Morris water maze test.

CONCLUSIONS

This observation demonstrated that hydrogen-rich saline peritoneal injection improves histologic and functional assessment in a rat model of CO encephalopathy. Hydrogen saline has potentials as a novel and alternative therapy for severely CO-poisoned patients with delayed neurologic sequelae. The therapeutic effects of hydrogen-rich saline may be related to antioxidant and anti-inflammatory actions.

摘要

目的

我们研究富氢盐水疗法对一氧化碳(CO)重度中毒后迟发性神经后遗症大鼠模型的可行性和疗效。

设计

对照动物研究。

地点

大学潜水医学研究实验室。

对象

体重 250±20 g 的 Sprague-Dawley 大鼠。

干预

大鼠在空气中暴露于 1000 ppm CO 40 分钟,然后暴露于 3000 ppm CO 20 分钟,直至失去意识。复苏后,大鼠分别于 0、12、24、36、48 和 60 小时时腹腔内注射富氢盐水或生理盐水(10 mL/kg),共 6 次。未 CO 中毒的大鼠作为正常对照组。

测量和主要结果

CO 中毒后 1 周观察到脑组织炎症、细胞死亡和认知功能障碍。与生理盐水治疗组相比,富氢盐水治疗组显著降低了降解髓鞘碱性蛋白的水平,降低了离子钙结合衔接分子 1、小胶质细胞标志物 Iba1、DNA 氧化以及促炎细胞因子白细胞介素-1β、白细胞介素-6 和肿瘤坏死因子-α的表达,在皮质和海马组织中。这些组织学和生物学的改善伴随着 Morris 水迷宫测试的改善。

结论

本观察表明,富氢盐水腹腔注射可改善 CO 脑病大鼠模型的组织学和功能评估。富氢盐水具有作为治疗 CO 中毒后迟发性神经后遗症的新型替代疗法的潜力。富氢盐水的治疗效果可能与抗氧化和抗炎作用有关。

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